The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Tumor necrosis factor (TNF) receptor type 1 ( p55) is a main mediator for TNF-alpha-induced skin inflammation.

Tumor necrosis factor alpha (TNF-alpha) is a pleiotropic proinflammatory cytokine that elicits a large number of biological effects, including inflammatory and immunoregulatory responses. Biological activities of TNF-alpha are mediated by two distinct TNF receptors, p55 type 1 receptor (TNFR1) and p75 type 2 receptor (TNFR2). To determine the role of TNF-alpha in the induction of inflammatory responses in the skin, gene-targeted mutant mice lacking either TNFR1 or TNFR2 were painted with irritant chemicals. Both phenol and croton oil painting onto the ears induced less inflammation in TNFR1(-) mice than normal and TNFR2(-) mice. Intradermal injection of TNF-alpha (0.2-200 ng for 3 days) into the ear induced less inflammation in TNFR1(-) mice than in normal mice. TNFR2(-) mice developed a normal inflammatory reaction to high doses of TNF-alpha (20-200 ng for 3 days), while they showed minimal reactivity to low doses of TNF-alpha (0.2-2 ng for 3 days). TNF-alpha is known to trigger the release of a series of other cytokines and to induce the expression of cell adhesion molecules, thus contributing to the development of inflammation. The levels of protein and mRNA for interleukin (IL)-6 were elevated in keratinocytes from normal as well as TNFR2(-) mice after treatment with TNF-alpha, while keratinocytes from TNFR1(-) mice did not show any up-regulation of IL-6. TNF-alpha induced intercellular adhesion molecule (ICAM)-1 expression in the keratinocytes from normal and TNFR2(-) mice, but not in those from TNFR1(-) mice. These results indicate that TNFR1 is critical for induction of skin inflammation by TNF-alpha.[1]


WikiGenes - Universities